Niwa O, Yokota Y, Ishida H, Sugahara T
Cell. 1983 Apr;32(4):1105-13. doi: 10.1016/0092-8674(83)90294-5.
Expression and DNA methylation of the Moloney murine leukemia virus (M-MuLV) genome were investigated in murine teratocarcinoma cells after virus infection. The newly acquired viral genome was devoid of methylation, yet its expression was repressed. The integrated viral genome in undifferentiated teratocarcinoma cells was methylated within 15 days after infection. Although 5-azacytidine decreased the level of DNA methylation, it did not activate M-MuLV in undifferentiated cells. Activation by 5-azacytidine occurred only in differentiated teratocarcinoma cells. Thus two independent mechanisms seem to regulate gene expression during the course of differentiation. The first mechanism operates in undifferentiated cells to block expression of M-MuLV and other exogeneously acquired viral genes, such as SV40 and polyoma virus, and does not depend on DNA methylation. The second mechanism relates only to differentiated cells and represses expression of genes in which DNA is methylated.
在病毒感染后的小鼠畸胎瘤细胞中，对莫洛尼鼠白血病病毒（M-MuLV）基因组的表达和DNA甲基化进行了研究。新获得的病毒基因组没有甲基化，但其表达受到抑制。未分化畸胎瘤细胞中的整合病毒基因组在感染后15天内发生甲基化。尽管5-氮杂胞苷降低了DNA甲基化水平，但它并未在未分化细胞中激活M-MuLV。5-氮杂胞苷的激活仅发生在分化的畸胎瘤细胞中。因此，在分化过程中似乎有两种独立的机制调节基因表达。第一种机制在未分化细胞中起作用，以阻断M-MuLV和其他外源获得的病毒基因（如SV40和多瘤病毒）的表达，且不依赖于DNA甲基化。第二种机制仅与分化细胞有关，并抑制DNA发生甲基化的基因的表达。
